Accumulating data indicates that periodontosis (localized juvenile periodontitis, LJP) is associated with a decrease in both polymorphonuclear leukocyte (PMN) chemotaxis and chemotactic receptor modulation. It may also be associated with a decrease in PMN phagocytosis. Ironically, chemotaxis, receptor modulation, and phagocytosis all depend on the coordinated reorganization of the actin cytoskeleton. Because ordered alterations of the actin cytoskeleton are so crucial to these three functions that relate to risk factors for LJP, we propose to examine the relationship between LJP and the ability of the PMN to polymerize actin. We raise the question: Does an inability of the PMN to appropriately polymerize an actin cytoskeleton upon stimulation reflect a central host defect in LJP? To examine this question we will compare the ability of PMNs from LJP and controls to polymerize actin upon stimulation.